In female B6D2F1 mice bearing an MXT‐M‐3,2 breast cancer graft the level of the phagocytic cells (e.g. of granulocytes and macrophages in the spleen and of granulocytes and monocytes in the blood) is significantly elevated. The positive correlation between the number of the phagocytic cells and the weight of the tumor indicates that the MXT‐M‐3,2 breast cancer promotes myelopoiesis, presumably by secretion of hematopoietic growth factors like GM‐CSF. This process can be described for each phagocyte type by a regression equation. Due to its hormonal potency [meso‐1,2‐bis(2,6‐dichloro‐ 4‐hydroxyphenyl)ethylenediamine]dichloroplatinum(II) (meso‐1‐PtCl2) can reduce the excessive numbers of the granulocytes and macrophages, which seem to be responsible for the progressive growth of the MXT‐M‐3,2 breast cancer. This process leads to an interruption of the vicious circle of mutual growth stimulation of breast cancer cells and these phagocytes. The target of meso‐1‐PtCl2 is the estrogen receptor (ER) of the breast cancer cell. The interaction between meso‐1‐PtCl2 and the ER presumably results in a diminished secretion of hematopoietic growth factors and hence in a decline of the number of phagocytic cells. Meso‐1‐PtCl2 does not inhibit the proliferation of tumor cells by direct interaction with their DNA, as is described for platinum complexes like cDDP. In its mode of action the equipotent, breast cancer inhibiting drug cDDP differs from meso‐1‐PtCl2. This is obvious from the fact that in cDDP‐ but not in meso‐1‐PtCl2‐treated, tumor bearing mice the number of granulocytes and macrophages does not markedly deviate from that in untreated control mice with tumors of the same weight. The drug cDDP probably does not interfere with the mechanism of the secretion of hematopoietic growth factors. The reduction of the number of tumor cells by cDDP leads to a decline of the number of phagocytic cells in accordance with the respective regression equations. In contrast to meso‐1‐PtCl2 and cDDP, ovariectomy causes elevated phagocyte numbers, probably due to the strongly reduced estrogen level. The studies described in this publication indicate that the anti‐breast cancer activity of meso‐1‐PtCl2 is caused by a decimation of phagocytes and with this by an abolition of the tumor promoting effect. Furthermore, a restoration of the natural immunosurveillance seems to be of importance.

中文翻译：

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[meso-1,2-bis (2,6-dichloro-4-hydroxyphenyl) ethylenediamine] dichloroplatinum (II) 是否作为免疫反应调节剂？IV. 标题化合物对渐进性生长的 MXT-M-3.2 乳腺癌对吞噬细胞的增殖增强作用的抑制

在携带 MXT - M - 3,2 乳腺癌移植物的雌性 B6D2F1 小鼠中，吞噬细胞的水平（例如脾脏中的粒细胞和巨噬细胞以及血液中的粒细胞和单核细胞）显着升高。吞噬细胞数量与肿瘤重量之间的正相关表明MXT-M-3,2乳腺癌促进骨髓细胞生成，推测可能是通过分泌GM-CSF等造血生长因子。可以通过回归方程为每种吞噬细胞类型描述该过程。由于其激素效力 [meso-1,2-bis (2,6-dichloro-4-hydroxyphenyl) ethylenediamine] dichloroplatinum (II) (meso-1-PtCl2) 可以减少粒细胞和巨噬细胞的过量数量，这似乎负责 MXT-M-3,2 乳腺癌的逐渐生长。这个过程导致乳腺癌细胞和这些吞噬细胞相互刺激生长的恶性循环的中断。meso ‐ 1 ‐ PtCl2 的靶标是乳腺癌细胞的雌激素受体 (ER)。meso - 1 - PtCl2 和 ER 之间的相互作用可能导致造血生长因子分泌减少，从而导致吞噬细胞数量下降。Meso ‐ 1 ‐ PtCl2 不会通过与肿瘤细胞的 DNA 直接相互作用来抑制肿瘤细胞的增殖，如 cDDP 等铂配合物所描述的那样。在作用方式上，等效的乳腺癌抑制药物 cDDP 与 meso - 1 - PtCl2 不同。这是显而易见的事实，在 cDDP- 但不是在 meso - 1 - PtCl2 - 处理，在携带肿瘤的小鼠中，粒细胞和巨噬细胞的数量与未治疗的具有相同重量的肿瘤的对照小鼠的数量没有显着差异。药物cDDP可能不会干扰造血生长因子的分泌机制。根据各自的回归方程，cDDP 导致肿瘤细胞数量减少导致吞噬细胞数量下降。与 meso ‐ 1 ‐ PtCl2 和 cDDP 相比，卵巢切除术会导致吞噬细胞数量增加，这可能是由于雌激素水平大大降低。该出版物中描述的研究表明，meso - 1 - PtCl2 的抗乳腺癌活性是由吞噬细胞的大量减少和肿瘤促进作用的消除引起的。此外，恢复自然免疫监视似乎很重要。